Estrogenic and hormonally-active environmental toxins from plastics, pesticides, animal feed, and cosmetics play a key role in precocious puberty—on the rise in young girls---as well many forms of cancer, says Dr. Devra Lee Davis, of the University of Pittsburgh’s new Center for Environmental Oncology.
PORTLAND, OR—Environmental toxins that mimic estrogen and other hormones are widespread in the environment, and they are key drivers of both precocious puberty in young girls, and reproductive system cancers later in life, according to Devra Lee Davis, PhD, MPH, Director of the Center on Environmental Oncology, University of Pittsburgh Cancer Center.
Speaking at the annual meeting of the American Holistic Medical Association, Dr. Davis stressed that, contrary to what many people believe, most cancers are not tied to any known hereditary defect. Even for cancers with recognized heritable mutations—breast cancer and the BRCA1 and 2 mutations, for instance—there are still many more people with the cancers than with the mutations. “Fewer than 1 in 10 women with breast cancer have one of the known ‘breast cancer genes.'”
Many arrows point toward environmental toxins rather than inherent genetic factors as the determining factor in cancer etiology. For one, cancer risk in adopted children tends to reflect that of their adoptive parents, not their biological parents, and fewer than half of all identical twins develop the same cancers. Migrants tend to develop the cancer risks of their new home countries rather than those of their countries of origin, said Dr. Davis, who is author of When Smoke Ran Like Water: Tales of Environmental Deception and the Battle Against Pollution (Basic Books), which won a National Book Award Bronze Medal in 2002.
Jane McElroy and colleagues at the University of Wisconsin published a case-control study last year in the Journal of the National Cancer Institute showing that the 254 women with breast cancer had consistently higher urinary cadmium levels than 246 age-matched control subjects who did not have the cancers.
There was a statistically significant increase in risk linked with increasing cadmium levels; women in the highest quartile for urine cadmium were 2.29 times more likely to have the cancer as those in the lowest quartile (McElroy JA, et al. J Natl Cancer Instit. 2006; 98(12): 869–873).
Cadmium gets into the bloodstream through three primary routes: cigarette smoke, consumption of food grown in contaminated soil, or drinking contaminated water. Cadmium in the water and soil ultimately comes from industrial waste.
At exposure levels of of 30–50 mcg per day cadmium has been linked to increased risk of bone fracture, cancer, kidney dysfunction and hypertension (Satarug S, et al. Toxicol Lett. 2003; 137(1–2): 65–83).
There is little doubt that heavy metals like cadmium and lead pose health risks. Far more controversial is the role of the so-called “endocrine disruptors” or estrogen mimics in the etiology of various diseases. Hormonally active toxins are ubiquitous these days, representing everything from pesticide residues to plasticizers and rubberizers. This is on top of all sorts of exogenous hormones to which we are all knowingly or unwittingly exposed.
The impact of endocrine disruptors goes a long way in explaining the consistent findings from studies of the health of farmers around the globe. While farmers tend to have overall better health than the non-farming population, presumably due to their increased physical activity and time spent outdoor, they also have consistently higher rates of cancer, especially cancers of the hematopoietic system, such as multlple myeloma, breast cancers, and reproductive system cancers. Farmers are typically exposed to much higher levels of pesticides, herbicides and other toxic chemicals many of which are endocrine disruptors.
Researchers have been reporting for over a decade that increasing numbers of girls are showing secondary sex development before the age of 10. Average age of puberty in girls has been steadily declining in most of the industrialized world. The trend is particularly strong for African-Americans.
Dr. Marcia Herman-Giddens at the University of North Carolina School of Public Health published a ground-shaking study in 1997 indicating that 27% of all African-American girls began developing breasts and pubic hair by age 7, and 48.3% reached this stage by age 8. Among White girls, the numbers were 6.7% and 14.7%, respectively. The mean age of menses was 12.2 years for the African American girls and 12.8 years for the Whites. The findings were based on data from more than 17,000 girls collected by 225 office-based pediatricians across the country (Herman-Giddens ME, et al. Pediatrics. 1997; 99(4): 505–512).
What was truly alarming about the study was the fact that 3% of the African-American girls and 1% of the White girls showed pubic hair and or breast development at age 3.
In a recent commentary in the International Journal of Andrology, Dr. Herman-Giddens noted that, “existing data on girls, particularly that for menarche, indicate that the trend for earlier sexual maturation has continued and that racial differences are significant, with African-American girls developing earlier than white girls.”
While data on boys are fewer and less reliable, the available numbers suggest boys may also be maturing earlier as well. She added that, “Earlier development may not be healthy and may indicate environmental problems that need to be further researched and addressed” (Herman-Giddens ME. Int J Androl. 2006; 29(1): 241–246).
Earlier onset of puberty could, in part, account for the higher incidence and mortality of breast cancer among premenopausal African-American versus White women. Lifetime estrogen exposure is a major risk factor for breast cancer in general; increased exposure during vulnerable periods like early childhood and pre-adolescence could definitely increase risk later in life, Dr. Davis said.
Wu and colleagues at the Department of Social and Preventive Medicine, State University of New York, Buffalo, analyzed NHANES data from 1988–1994, tracking sexual development among three racial/ethnic cohorts: African-Americans, Mexican-Americans, and White Euro-Americans. African-American girls enter puberty earliest, followed by Mexican-Americans, and then Whites. By age 9, 49% of African-American girls show breast development, compared with only 24.5% of Mexican Americans, and 15.8% of the Whites (Wu T, et al. Pediatrics. 2002; 110(4): 752–757).
The early puberty trend among girls is related to the increasing prevalence of childhood obesity. Researchers at Virginia Commonweath University studied a large cohort of 6–9 year old girls, comparing mean age-adjusted body mass indices between girls who had breast or pubic hair development and those who did not. Among the White girls, there was a clear association: those who showed secondary sexual development had consistently higher BMIs. Among the Black girls, there was also an association, but it was weaker, and only statistically significant for the 9-year-olds (Kaplowitz PB, et al. Pediatrics. 2001; 108(2): 347–353).
They concluded that while obesity seems to be a contributing factor for early puberty, the lack of a strong correlation in Blacks, and the markedly higher early puberty rates in African-American communities suggest that environmental factors and hereditary differences play a central role. In Wu’s analysis, the racial differences in puberty onset remained even after the investigators adjusted for BMI and socio-economic variables.
Dr. Davis is convinced exposure to endocrine-disrupting compounds in the environment play a central role in the early puberty trend. With the increased use of hormone-modulating drugs, hormone-containing cosmetics, hormones to promote growth of livestock, hormone-based pesticides, and hormone-mimicking industrial pollutants, we are living in an increasingly hormonized world.
Shortly after Dr. Herman-Giddens’ study, Dr. Chandra Tiwary, then at the Brooke Army Medical Center, Ft. Sam Houston, published a case series involving four African-American girls aged 14–93 months, who all showed breast development and pubic hair. All were regularly exposed to shampoos or personal care products containing placental extracts or other estrogenic compounds. Such products are widespread in the consumer market, and especially popular in African-American communities. The premature thelarche regressed on discontinuation of these products.
Dr. Tiwary, now at the University of Pennsylvania, tried estrogen-containing shampoos himself for several weeks and found they could, indeed, modulate serum sex hormone levels.
It is easy to target hormone-containing personal care products and eliminate them either by refusing to use them personally or to push for regulatory action. It is far more difficult to deal with the challenge of endocrine disrupting pollutants, a far bigger concern, says Dr. Davis.
Girls in Puerto Rico showing premature breast growth had a six-fold higher serum concentration of total phthalate esters, byproducts of certain types of plastic, compared with normal girls (Colon I, et al. Environ Health Perspect. 2000; 108(9): 895–900). Puerto Rico has among the highest reported incidence rates of premature breast development; it is also a place with very high levels of pesticide and plastic pollution.
According to Dr. Davis, total lifetime exposure to unbound steroid hormones, especially estrogen, is the common link between most known risk factors for breast and reproductive system cancers. Girls who reach puberty early and are exposed throughout their lives to a complex cocktail of estrogenic compounds in their environments would, presumably be, at increased risk for breast and reproductive system cancers.
Exposure to endocrine-disrupting toxins has damaging effects on males as well, said Dr. Davis. Sperm counts are declining, and testicular cancers are increasing as are male birth defects. These are all related and may be connected to early life exposure to hormonally active toxins. Sertoli cells are differentiated and programmed during the first trimester of gestation. If they are damaged by toxic exposures at that stage, their function is compromised later in life.
Reproductive system cancers are an obvious concern, but she stressed that other types of cancer are also hormonally sensitive, something many physicians do not realize. For example, Lung cancers are not typically thought of as hormonally-mediated cancers. But in reality, lung cancer cells have a lot of estrogen receptors on their surfaces, and they are highly sensitive to estrogen signals. Lung tumor cell lines exposed to various endocrine-disrupting chemicals show consistently higher growth rates, enhanced cell migration, and a troubling resistance to cisplatin.
Dr. Davis believes women may be especially vulnerable to lung neoplasms because, in addition to whatever external carcinogens they may encounter, they’ve got a constant stream of estrogen that could be potentiating the tumors.
It is the mixtures of multiple potential carcinogens and their possible interactions with natural phyisiology that most concerns Dr. Davis and other environmental health scientists. While certain toxins like bisphenol A or polychlorinated biphenyls often grab the headlines, it may very well be the total burden of multiple chemical toxins, combined with poor diet, stress, livestyle and socioeconomic factors that are the critical determinants.
Still, many environmental toxins are unnecessary risks, and Dr. Davis believes the medical community has a public health obligation to work toward eliminating as many of these as possible. The Center for Environmental Ecology which she heads, has as its mission, the identification of controllable or avoidable causes of cancer linked with the environment and to create tools and interventions that inform, educate and change individual and institutional behaviors.
Of course, this is an uphill struggle. “There’s billions invested in doing things the old way.”
Her guiding light is the so-called precautionary principle, the idea that even without definitive, prospective evidence proving that a chemical causes disease, it is reasonable to stop or limit its use if there’s a substantial amount of epidemiologic, case-control, animal and cell culture data indicating real potential for harm. In other words, “better safe than sorry.” She and many environmental scientists believe this perspective is sorely lacking in US regulations. “Do we really need to wait until we have definitive proof of harm before we come up with safer things?”
In 2003, the City of San Francisco, which formally adopted the precautionary principle as a guideline for all city legislation, acknowledging that the public has a right to know about any potentially harmful toxins in the environment, and that government has the obligation to inform and protect the public, while establishing policy to promote development of safe alternatives to current toxins.
Dr. Davis also applauded the work of Health Care Without Harm, Hospitals for a Healthy Environment and the many thousands of physicians, nurses and hospital administrators working effectively to minimize the use of mercury, polyvinyl chloride, toxic solvents and other toxic substances in clinical practice. She urged physicians to remember that, “The things you use in your offices have effects well beyond your offices. Choose wisely.”
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